Ординатура / Офтальмология / Английские материалы / Clinical Ophthalmology A Systematic Approach 7th Edition_Kanski, Bowling_2011

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Fig. 18.9 Diagnostic positions of gaze

Laws of ocular motility

1Agonist–antagonist pairs are muscles of the same eye that move the eye in opposite directions. The agonist is the primary muscle moving the eye in a given direction. The antagonist acts in the opposite direction to the agonist. For example the right lateral rectus is the antagonist to the right medial rectus.

2Synergists are muscles of the same eye that move the eye in the same direction. For example, the right superior rectus and right inferior oblique act synergistically in elevation.

3Yoke muscles (contralateral synergists) are pairs of muscles, one in each eye, that produce conjugate ocular movements. For example, the yoke muscle of the left superior oblique is the right inferior rectus.

4Sherrington law of reciprocal innervation (inhibition) states that increased innervation to an extraocular muscle (e.g. right medial rectus) is accompanied by a reciprocal decrease in innervation to its antagonist (e.g. right lateral rectus; Fig. 18.10). This means that when the medial rectus contracts the lateral rectus automatically relaxes and vice versa. The Sherrington law applies to both versions and vergences.

5Hering law of equal innervation states that during any conjugate eye movement, equal and simultaneous innervation flows to the yoke muscles (Fig. 18.11).

•In the case of a paretic squint, the amount of innervation to both eyes is symmetrical, and always determined by the fixating eye, so that the angle of deviation will vary according to which eye is used for fixation.

•For example if, in the case of a left lateral rectus palsy, the right normal eye is used for fixation, there will be an inward deviation of the left eye due to the unopposed action of the antagonist of the paretic left lateral rectus (left medial rectus). The amount of misalignment of the two eyes in this situation is called the primary deviation (Fig. 18.12, left).

•If the paretic left eye is now used for fixation, additional innervation will flow to the left lateral rectus, in order to establish this. However, according to Hering law, an equal amount of innervation will also flow to the right medial rectus (yoke muscle). This will result in an overaction of the right medial rectus and an excessive amount of adduction of the right eye.

•The amount of misalignment between the two eyes in this situation is called the secondary deviation (Fig. 18.12, right). In a paretic squint, the secondary deviation exceeds the primary deviation.

6Muscle sequelae are the effects of the interactions described by these laws. They are of prime importance in diagnosing ocular motility disorders and in particular in distinguishing a recently acquired from a longstanding palsy (see clinical evaluation). The full pattern of changes takes time to develop and can be summarized as follows:

•Primary underaction (e.g. left superior oblique).

•Secondary overaction of the contralateral synergist or yoke muscle (right IR; Hering law).

•Secondary overaction and later contracture of the unopposed ipsilateral antagonist (left IO; Sherrington law).

•Secondary inhibition of the contralateral antagonist (right SR; Hering and Sherrington laws).

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Fig. 18.10 Sherrington law of reciprocal innervation

Fig. 18.11 Hering law of equal innervation of yoke muscles

Fig. 18.12 Primary and secondary deviations in paretic strabismus

Sensory considerations

Basic aspects

1Normal binocular single vision (BSV) involves the simultaneous use of both eyes with bifoveal fixation, so that each eye contributes to a common single perception of the object of regard. This represents the highest form of binocular cooperation. Conditions necessary for normal BSV are:

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•Normal routing of visual pathways with overlapping visual fields.

•Binocularly driven neurones in the visual cortex.

•Normal retinal (retinocortical) correspondence (NRC) resulting in cyclopean viewing.

•Accurate neuromuscular development and coordination, so that the visual axes are directed at, and maintain fixation on, the object of regard.

•Approximately equal image clarity and size for both eyes.

•BSV is based on NRC which requires first an understanding of uniocular visual direction and projection.

2Visual direction is the projection of a given retinal element in a specific direction in subjective space.

aPrincipal visual direction is the direction in external space interpreted as the line of sight. This is normally the visual direction of the fovea and is associated with a sense of direct viewing.

bSecondary visual directions are the projecting directions of extrafoveal points with respect to the principal direction of the fovea, associated with indirect (eccentric) viewing.

3Projection is the subjective interpretation of the position of an object in space on the basis of stimulated retinal elements.

•If a red object stimulates the right fovea (F), and a black object which lies in the nasal field stimulates a temporal retinal element (T), the red object will be interpreted by the brain as having originated from the straight ahead position and the black object will be interpreted as having originated in the nasal field (Fig. 18.13A). Similarly, nasal retinal elements project into the temporal field, upper retinal elements into the lower field and vice versa.

•With both eyes open, the red fixation object is now stimulating both foveae, which are corresponding retinal points. The black object is now not only stimulating the temporal retinal elements in the right eye but also the nasal elements of the left eye. The right eye therefore projects the object into its nasal field and the left eye projects the object into its temporal field.

•Because both of these retinal elements are corresponding points, they will both project the object into the same position in space (the left side) and there will be no double vision.

4Retinomotor values

•The image of an object in the peripheral visual field falls on an extrafoveal element. To establish fixation on this object a saccadic version of accurate amplitude is required.

•Each extrafoveal retinal element therefore has a retinomotor value proportional to its distance from the fovea, which guides the amplitude of saccadic movements required to ‘look at it’.

•Retinomotor value, zero at the fovea, increases progressively towards the retinal periphery.

5Corresponding ‘points’ are areas on each retina that share the same subjective visual direction (for example, the foveae share the primary visual direction).

•Points on the nasal retina of one eye have corresponding points on the temporal retina of the other eye and vice versa. For example, an object producing images on the right nasal retina and the left temporal retina will be projected into the right side of visual space. This is the basis of normal retinal correspondence.

•This retinotopic organization is reflected back along the visual pathways, each eye maintaining separate images until the visual pathways converge onto binocularly responsive neurones in the primary visual cortex.

6The horopter is an imaginary plane in external space, relative to both the observer's eyes for a given fixation target, all points on which stimulate corresponding retinal elements and are therefore seen singly and in the same plane (Fig. 18.13B). This plane passes through the intersection of the visual axes and therefore includes the point of fixation in BSV.

7Panum fusional space (‘volume’) is a zone in front of and behind the horopter in which objects stimulate slightly non-corresponding retinal points (retinal disparity).

•Objects within the limits of the fusional space are seen singly and the disparity information is used to produce a perception of binocular depth (stereopsis). Objects in front of and behind Panum space appear double.

•This is the basis of physiological diplopia. Panum space is shallow at fixation (6 seconds of arc) and deeper towards the periphery (30–40 seconds of arc at 15° from the fovea).

•The retinal areas stimulated by images falling within Panum fusional space are termed Panum fusional areas.

•Therefore objects on the horopter are seen singly and in one plane. Objects in Panum fusional areas are seen singly and stereoscopically. Objects outside Panum fusional areas appear double.

•Physiological diplopia is usually accompanied by physiological suppression.

8BSV is characterized by the ability to fuse the images from the two eyes and to perceive binocular depth:

aSensory fusion involves the integration by the visual areas of the cerebral cortex of two similar images, one from each eye, into one image. It may be central, which integrates the image falling on the foveae, or peripheral, which integrates parts of the image falling outside the foveae. It is possible to maintain fusion with a central visual deficit in one eye, but peripheral fusion is essential to BSV and may be affected in patients with advanced field changes in glaucoma and pituitary lesions.

bMotor fusion involves the maintenance of motor alignment of the eyes to sustain bifoveal fixation. It is driven by retinal image disparity, which stimulates fusional vergences.

9Fusional vergence involves disjugate eye movements to overcome retinal image disparity. Fusional vergence amplitudes can be measured with prisms or on the synoptophore. Normal values are:

•Cyclovergence: about 2–3°.

Fusional convergence helps to control an exophoria whereas fusional divergence helps to control an esophoria. The fusional

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vergence mechanism may be decreased by fatigue or illness, converting a phoria to a tropia. The amplitude of fusional vergence mechanisms can be improved by orthoptic exercises, particularly in the case of near fusional convergence for the relief of convergence insufficiency.

10Stereopsis is the perception of depth. It arises when objects behind and in front of the point of fixation (but within Panum fusional space) stimulate horizontally disparate retinal elements simultaneously. The fusion of these disparate images results in a single visual impression perceived in depth. A solid object is seen stereoscopically (in 3D) because each eye sees a slightly different aspect of the object.

11Sensory perceptions. At the onset of a squint two sensory perceptions arise based on the normal projection of the retinal areas stimulated; confusion and pathological diplopia may result. These require simultaneous visual perception i.e. the ability to perceive images from both eyes simultaneously. Young children readily suppress diplopia but it is persistent and usually troublesome in strabismus in older children and adults, when it arises after the sensitive period for binocularity (see below).

aConfusion is the simultaneous appreciation of two superimposed but dissimilar images caused by stimulation of corresponding retinal points (usually the foveae) by images of different objects (Fig. 18.14).

bPathological diplopia is the simultaneous appreciation of two images of the same object in different positions and results from images of the same object falling on non-corresponding retinal points.

•In esotropia the diplopia is homonymous (uncrossed – Fig. 18.15A).

•In exotropia the diplopia is heteronymous (crossed – Fig. 18.15B).

Fig. 18.13 Principles of projection

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Fig. 18.14 Confusion

Fig. 18.15 Diplopia. (A) Homonymous (uncrossed) diplopia in right esotropia with normal retinal correspondence; (B) heteronymous (crossed) diplopia in right exotropia with normal retinal correspondence

Sensory adaptations to strabismus

The ocular sensory system in children has the ability to adapt to anomalous states (confusion and diplopia) by two mechanisms: (a) suppression and (b) abnormal retinal correspondence (ARC). These occur because of the plasticity of the developing visual system in

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children under the age of 6–8 years. Occasional adults who develop sudden-onset strabismus are able to ignore the second image after a time and therefore do not complain of diplopia.

Suppression

Suppression involves active inhibition by the visual cortex of the image from one eye when both eyes are open. Stimuli for suppression include diplopia, confusion and a blurred image from one eye resulting from astigmatism/anisometropia. Clinically, suppression may be:

1Central or peripheral. In central suppression the image from the fovea of the deviating eye is inhibited to avoid confusion. Diplopia, on the other hand, is eradicated by the process of peripheral suppression, in which the image from the peripheral retina of the deviating eye is inhibited.

2Monocular or alternating. Suppression is monocular when the image from the dominant eye always predominates over the image from the deviating (or more ametropic) eye, so that the image from the latter is constantly suppressed. This type of suppression leads to amblyopia. When suppression alternates (switches from one eye to the other) amblyopia is less likely to develop.

3Facultative or obligatory. Facultative suppression occurs only when the eyes are misaligned. Obligatory suppression is present at all times, irrespective of whether the eyes are deviated or straight. Examples of faculative suppression include intermittent exotropia and Duane syndrome.

Abnormal retinal correspondence

Abnormal retinal correspondence (ARC) is a condition in which non-corresponding retinal elements acquire a common subjective visual direction, i.e. fusion occurs in the presence of a small angle manifest squint.

•The fovea of the fixating eye is thus paired with a non-foveal element of the deviated eye.

•ARC is a positive sensory adaptation to strabismus (as opposed to negative adaptation by suppression), which allows some anomalous binocular vision in the presence of a heterotropia.

•Binocular responses in ARC are never as good as in normal bifoveal BSV. ARC is most frequently present in small angle esotropia (microtropia) associated with anisometropia.

Microtropia

Microtropia is a small angle (<10 Δ) squint in which stereopsis is present but reduced, and there is relative amblyopia of the more ametropic eye. Microtropia has two forms.

1In microtropia with identity the point used for monocular fixation by the squinting eye corresponds with the fovea of the straight eye under binocular viewing conditions. Therefore on cover test there is no movement of the squinting eye when it takes up monocular fixation.

2In microtropia without identity the monocular fixation point of the squinting eye does not correspond with the fovea of the straight eye in binocular viewing. There is therefore a small movement of the deviating eye when it takes up monocular fixation on cover testing. ARC is less common in accommodative esotropia because of the variability of the angle of deviation, or in large angle deviations because the separation of the images is too great.

Consequences of strabismus

•The fovea of the squinting eye is suppressed to avoid confusion.

•Diplopia will occur, since corresponding retinal elements receive different images.

•To avoid diplopia, the patient will develop either peripheral suppression of the squinting eye or ARC.

•If constant unilateral suppression occurs this will subsequently lead to strabismic amblyopia.

Motor adaptation to strabismus

Motor adaptation involves the adoption of an abnormal head posture (AHP) and occurs primarily in children with congenitally abnormal eye movements who use the AHP to maintain BSV. In these children loss of an AHP may indicate loss of binocular function and the need for surgical intervention. These patients may present in adult life with symptoms of decompensation, often unaware of their AHP. Acquired paretic strabismus in adults may be consciously controlled by an AHP provided the deviation is neither too large nor too variable with gaze (incomitance). The AHP eliminates diplopia and helps to centralize the binocular visual field. The patient will turn the head into the direction of the field of action of the weak muscle, so that the eyes are then automatically turned the opposite direction and as far as possible away from its field of action (i.e. the head will turn where the eye cannot). An AHP is analyzed in terms of the following three components:

•Face turn to right or left.

•Head tilt to right or left.

•Chin elevation or depression.

1A face turn will be adopted to control a purely horizontal deviation. For example, if the left lateral rectus is paralyzed, diplopia will occur in left gaze; the face will be turned to the left which deviates the eyes to the right away from the field of action of the weak muscle and area of diplopia. A face turn may also be adopted in a paresis of a vertically acting muscle to avoid the side where the vertical deviation is greatest (e.g. in a right superior oblique weakness the face is turned to the left).

2A head tilt is adopted to compensate for torsional and/or vertical diplopia. In a right superior oblique weakness, the right eye is relatively elevated and the head is tilted to the left (Fig. 18.16), towards the hypotropic eye; this reduces the vertical separation of the diplopic images and permits fusion to be regained. If there is a significant torsional component preventing fusion, tilting the head in the same left direction will reduce this by invoking the righting reflexes (placing the extorted right eye in a position which requires extorsion).

3Chin elevation or depression may be used to compensate for weakness of an elevator or depressor muscle or to minimize the horizontal deviation when an A or V pattern is present.

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Fig. 18.16 Compensatory head posture in a right 4th nerve palsy

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Amblyopia

Classification

Amblyopia is the unilateral, or rarely bilateral, decrease in best-corrected visual acuity caused by form vision deprivation and/or abnormal binocular interaction, for which there is no identifiable pathology of the eye or visual pathway.

1Strabismic amblyopia results from abnormal binocular interaction where there is continued monocular suppression of the deviating eye.

2Anisometropic amblyopia is caused by a difference in refractive error between the eyes and may result from a difference of as little as 1.0 D sphere. The more ametropic eye receives a blurred image, in a mild form of visual deprivation. It is frequently associated with microstrabismus and may coexist with strabismic amblyopia.

3Stimulus deprivation amblyopia results from vision deprivation. It may be unilateral or bilateral and is caused by opacities in the media (e.g. cataract) or ptosis which covers the pupil.

4Bilateral ametropic amblyopia results high symmetrical refractive errors, usually hypermetropia.

5Meridional amblyopia results from image blur in one meridian. It can be unilateral or bilateral and is caused by uncorrected astigmatism (usually >1 D) persisting beyond the period of emmetropization in early childhood.

Diagnosis

In the absence of an organic lesion, a difference in best corrected visual acuity of two Snellen lines or more (or >1 log unit) is indicative of amblyopia. Visual acuity in amblyopia is usually better when reading single letters than letters in a row. This ‘crowding’ phenomenon occurs to a certain extent in normal individuals but is more marked in amblyopes and must be taken into account when testing preverbal children.

Treatment

It is essential to examine the fundi to diagnose any visible organic disease prior to commencing treatment for amblyopia. Organic disease and amblyopia may coexist and a trial of patching may still be indicated in the presence of organic disease. If acuity does not respond to treatment, investigations such as electrophysiology or imaging should be reconsidered. The sensitive period during which acuity of an amblyopic eye can be improved is usually up to 7–8 years in strabismic amblyopia and may be longer (into teens) for anisometropic amblyopia where good binocular function is present.

1Occlusion of the normal eye, to encourage use of the amblyopic eye, is the most effective treatment. The regimen, full-time or parttime, depends on the age of the patient and the density of amblyopia.

•The younger the patient the more rapid the likely improvement although the greater the risk of inducing amblyopia in the normal eye. It is therefore very important to monitor visual acuity regularly in both eyes during treatment.

•The better the visual acuity at the start of occlusion, the shorter the duration required, although there is wide variation between patients.

•If there has been no improvement after 6 months of effective occlusion, further treatment is unlikely to be fruitful.

•Poor compliance is the single greatest barrier to improvement and must be monitored. Amblyopia treatment benefits from time spent at the outset on communication of the rationale and the difficulties involved.

2Penalization, in which vision in the normal eye is blurred with atropine, is an alternative method. It is best in the treatment of relatively mild amblyopia (6/24 or better) in association with hypermetropia. Conventional occlusion is likely to produce a quicker response than atropine which is generally used when compliance with occlusion is poor.

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Clinical evaluation

History

1Age of onset.

•The earlier the onset, the more likely the need for surgical correction.

•The later the onset, the greater the likelihood of an accommodative component (mostly arising between 18–36 months).

•The longer the duration of squint in early childhood the greater the risk of amblyopia, unless fixation is freely alternating. Inspection of previous photographs may be useful for the documentation of strabismus or an AHP.

2Symptoms may indicate decompensation of a pre-existent heterophoria or more significantly a recently acquired (usually paretic) condition. In the former, the patient usually complains of discomfort, blurring and possibly diplopia of indeterminate onset and duration compared to the acquired condition with the sudden onset of diplopia.

•The type of diplopia (horizontal, cyclovertical) should be established, the direction of gaze in which it predominates and whether any BSV is retained.

•In adults it is very important to determine exactly what problems the squint is causing as a basis for decisions about treatment.

•It is not unusual for patients to present with spurious symptoms which mask embarrassment over a cosmetically noticeable squint.

3Variability is significant because intermittent strabismus indicates some degree of binocularity. An equally alternating deviation suggests symmetrical visual acuity in both eyes.

4General health or developmental problems may be significant (e.g. children with cerebral palsy have an increased incidence of strabismus). In older patients poor health and stress may cause decompensation, and in acquired paresis patients may report associations or causal factors (trauma, neurological disease, diabetes etc).

5Birth history, including period of gestation, birth weight and any problems in utero, with delivery or in the neonatal period.

6Family history is important because strabismus is frequently familial, although there is no definitive inheritance pattern. It is also important to know what therapy was necessary in other family members.

7Previous ocular history including refractive prescription and compliance with spectacles or occlusion, previous surgery or prisms is important to future treatment options and prognosis.

Visual acuity

Testing in preverbal children

The evaluation can be separated into the qualitative assessment of visual behaviour and the quantitative assessment of visual acuity using preferential looking tests. Assessment of visual behaviour is achieved as follows:

1Fixation and following may be assessed using bright attention-grabbing targets (a face is often best). This method indicates whether the infant is visually alert and is of particular value in a child suspected of being blind.

2Comparison between the behaviour of the two eyes may reveal a unilateral preference. Occlusion of one eye, if strongly objected to by the child, indicates poorer acuity in the other eye. However, it is possible to have good visual attention with each eye but unequal visual acuity and all risk factors for amblyopia must be considered in the interpretation of results.

3Fixation behaviour can be used to establish unilateral preference if a manifest squint is present.

aFixation is promoted in the squinting eye by occluding the dominant eye while the child fixates a target of interest (preferably incorporating a light).

b Fixation is then graded as central or non-central and steady or unsteady (the corneal reflection can be observed).

cThe other eye is then uncovered and the ability to maintain fixation is observed.

d If fixation immediately returns to the uncovered eye, then visual acuity is probably impaired. e If fixation is maintained through a blink, then visual acuity is probably good.

fIf the patient alternates fixation, then the two eyes have equal vision.

4The 10 test is similar and can be used regardless of whether a manifest squint is present. It involves the promotion of diplopia using a 10 vertical prism. Alternation between the diplopic targets suggests equal visual acuity.

5 Rotation test is a gross qualitative test of the ability of an infant to fixate with both eyes open. The test is performed as follows: a The examiner holds the child facing him and rotates briskly through 360°.

bIf vision is normal, the eyes will deviate in the direction of rotation under the influence of the vestibulo-ocular response. The eyes flick back to the primary position to produce a rotational nystagmus.

cWhen rotation stops, nystagmus is briefly observed in the opposite direction for 1–2 seconds and should then cease due to suppression of post-rotary nystagmus by fixation.

dIf vision is severely impaired, the post-rotation nystagmus does not stop as quickly when rotation ceases because the vestibulo-ocular response is not blocked by visual feedback.

6Preferential looking tests can be used from early infancy and are based on the fact that infants prefer to look at a pattern rather

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than a homogeneous stimulus. The infant is exposed to a stimulus and the examiner observes the eyes for fixation movements, without themselves knowing the stimulus position.

•Tests which are in common use include the Teller or Keeler acuity cards, which consist of black stripes (gratings) of varying widths, and Cardiff acuity cards, which consist of familiar pictures with variable outline width (Fig. 18.17).

•Low frequency (coarse) gratings or pictures with a wider outline are seen more easily than high frequency gratings or thin outline pictures, and an assessment of resolution (not recognition) visual acuity is made accordingly.

•Since grating acuity often exceeds Snellen acuity in amblyopia, Teller cards may overestimate visual acuity. These methods may not be reliable if a proper forced-choice staircase protocol is not followed during testing and neither method has high sensitivity to the presence of amblyopia. The results must be considered in combination with risk factors for amblyopia.

7Pattern visual evoked potentials (VEP) give a representation of spatial acuity but are more commonly used in the diagnosis of optic neuropathy.

Fig. 18.17 Cardiff acuity cards

Testing in verbal children

All of the tests described below are performed at 3 or 4 metres at which it is easier to obtain compliance than at 6 metres, with little or no clinical detriment. It is important to note that amblyopia can only be accurately diagnosed using a crowded test requiring target recognition and that logMAR tests (logarithm of the minimal angle of resolution) provide the best measure against which improvement with amblyopia therapy can be assessed. These are readily available in formats suited to normal children from 2 years onwards.

1At age 2 years, most children will have sufficient language skills to undertake a picture naming test such as the crowded Kay pictures (Fig. 18.18A).

2At age 3 years, most children will be able to undertake the matching of letter optotypes as in the Keeler logMAR (Fig. 18.18B) or Sonksen crowded tests. If a crowded letter test proves too difficult it is preferable to perform the crowded Kay pictures than to use single optotype letters.

3Older children may continue with the crowded letter tests, naming or matching them; LogMAR tests are in common usage and are preferable to Snellen for all children at risk of amblyopia.

Fig. 18.18 (A) Kay pictures; (B) Keeler logMARcrowded test

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